Abstract

Objective: To determine whether there is a relation between impairment of lung diffusion and reduced exercise capacity in chronic heart failure.

Design: 40 patients with heart failure in stable clinical condition and 40 controls participated in the study. All subjects underwent standard pulmonary function tests plus measurements of resting lung diffusion (carbon monoxide transfer, Tlco), pulmonary capillary volume (Vc), and membrane resistance (Dm), and maximal cardiopulmonary exercise testing. In 20 patients and controls, the following investigations were also done: (1) resting and constant work rate Tlco; (2) maximal cardiopulmonary exercise testing with inspiratory O₂ fractions of 0.21 and 0.16; and (3) rest and peak exercise blood gases. The other subjects underwent Tlco, Dm, and Vc measurements during constant work rate exercise.

Results: In normoxia, exercise induced reductions of haemoglobin O₂ saturation never occurred. With hypoxia, peak exercise uptake (peak V̇o₂) decreased from (mean (SD)) 1285 (395) to 1081 (396) ml/min (p < 0.01) in patients, and from 1861 (563) to 1771 (457) ml/min (p < 0.05) in controls. Resting Tlco correlated with peak V̇o₂ in heart failure (normoxia < hypoxia). In heart failure patients and normal subjects, Tlco and peak V̇o₂ correlated with O₂ arterial content at rest and during peak exercise in both normoxia and hypoxia. Tlco, Vc, and Dm increased during exercise. The increase in Tlco was greater in patients who had a smaller reduction of exercise capacity with hypoxia. Alveolar–arterial O₂ gradient at peak correlated with exercise capacity in heart failure during normoxia and, to a greater extent, during hypoxia.

Conclusions: Lung diffusion impairment is related to exercise capacity in heart failure.